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You searched for +publisher:"University of Texas Medical Branch – Galveston" +contributor:("Giulio Taglialatela, PhD"). Showing records 1 – 2 of 2 total matches.

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University of Texas Medical Branch – Galveston

1. [No author]. Critical role of ROS in capsaicin-induced hyperalgesia .

Degree: 2008, University of Texas Medical Branch – Galveston

Recent studies indicate that reactive oxygen species (ROS) are critically involved in persistent pain primarily through spinal mechanisms, thus suggesting ROS involvement in central sensitization. To investigate ROS involvement in central sensitization, the effects of ROS scavengers and donors on pain behaviors were examined in mice. The capsaicin-induced hyperalgesia was used as a pain model since it has 2 distinctive pain components, primary and secondary hyperalgesia representing peripheral and central sensitization, respectively. Foot withdrawal frequencies in response to von Frey filament stimuli were measured and used as an indicator of mechanical hyperalgesia. The production of mitochondrial ROS was examined by using a ROS sensitive dye MitoSox-Red. Mice developed primary and secondary mechanical hyperalgesia after capsaicin injection. A systemic or intrathecal ROS scavenger treatment significantly reduced secondary hyperalgesia, but not primary hyperalgesia, in a dose dependent manner. MitoSox positive dorsal horn neuron numbers were increased significantly after capsaicin treatment. This study suggests that ROS mediates the development and maintenance of capsaicin-induced hyperalgesia in mice, mainly through central sensitization and the elevation of spinal ROS is most likely due to increased production of mitochondrial superoxides in dorsal horn neurons. \r\nThis study also investigated the role of mitochondrial antioxidant SOD2 in pain. Experiments were done to measure spinal levels of SOD2 protein and activity, inactivated SOD2 protein, and ROS accumulating dorsal horn cells after capsaicin injection to mouse foot with or without ROS scavengers. The capsaicin-induced hyperalgesia was determined in mice after manipulating SOD levels. Results showed that following capsaicin treatment, spinal levels of SOD2 activity were decreased, inactivated SOD2 proteins were increased, but total SOD2 proteins were unchanged. These changes were reversed with ROS scavengers. Mice showed enhanced or reduced hyperalgesia with decreased or increased SOD2 levels, respectively. The number of ROS accumulating cells was increased in SOD2KO mice but decreased in SOD2Tg mice. The data suggest that SOD2 activity levels determine the ROS accumulation, which in turn determines the levels of central sensitization and capsaicin-induced secondary hyperalgesia. Therefore, this study suggests a therapeutic potential of targeting SOD2 in persistent pain conditions. \r\n\r\n\r\n Advisors/Committee Members: Jin Mo Chung, PhD (advisor), William Willis, MD PhD (committeeMember), Kyungsoon Chung, PhD (committeeMember), Giulio Taglialatela, PhD (committeeMember), Eric Klann, PhD (committeeMember).

Subjects/Keywords: SOD-2; ROS; persistent pain; central sensitization

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

author], [. (2008). Critical role of ROS in capsaicin-induced hyperalgesia . (Thesis). University of Texas Medical Branch – Galveston. Retrieved from http://hdl.handle.net/2152.3/33

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

author], [No. “Critical role of ROS in capsaicin-induced hyperalgesia .” 2008. Thesis, University of Texas Medical Branch – Galveston. Accessed October 22, 2017. http://hdl.handle.net/2152.3/33.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

author], [No. “Critical role of ROS in capsaicin-induced hyperalgesia .” 2008. Web. 22 Oct 2017.

Vancouver:

author] [. Critical role of ROS in capsaicin-induced hyperalgesia . [Internet] [Thesis]. University of Texas Medical Branch – Galveston; 2008. [cited 2017 Oct 22]. Available from: http://hdl.handle.net/2152.3/33.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

author] [. Critical role of ROS in capsaicin-induced hyperalgesia . [Thesis]. University of Texas Medical Branch – Galveston; 2008. Available from: http://hdl.handle.net/2152.3/33

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation


University of Texas Medical Branch – Galveston

2. [No author]. Regional and temporal differential regulation of the N-methyl-D-aspartate receptor by phencyclidine during development .

Degree: 2005, University of Texas Medical Branch – Galveston

Disruptions in glutamatergic neurotransmission may play a role in the pathogenesis of schizophrenia. The purpose of this study was to determine phencyclidine (PCP)-induced changes in the NMDA receptor subunit composition and the relationship of these changes to the deficits in pre-pulse inhibition (PPI) caused by PCP treatment. Postnatal rats were treated with atypical or typical antipsychotics or selective dopamine or serotonin receptor antagonists prior to acute or sub-chronic PCP. This study provides evidence that two distinct mechanisms underlie effects of acute and sub-chronic PCP on NMDA receptor subunit up-regulation. Furthermore, we discovered that D1, D2, and 5-HT2A receptors play a pivotal role in sub-chronic PCP-induced up-regulation of NR1 and NR2A. Finally, we were able to correlate changes in NMDA receptor subunits to the behavioral effects of PCP in this animal model of schizophrenia. Advisors/Committee Members: Kenneth M. Johnson, PhD (advisor), Kathryn Cunningham, PhD. (committeeMember), Giulio Taglialatela, PhD. (committeeMember), Geoffrey T. Swanson (committeeMember).

Subjects/Keywords: schizophrenia; olanzapine; animal model

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6th Edition):

author], [. (2005). Regional and temporal differential regulation of the N-methyl-D-aspartate receptor by phencyclidine during development . (Thesis). University of Texas Medical Branch – Galveston. Retrieved from http://hdl.handle.net/2152.3/170

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16th Edition):

author], [No. “Regional and temporal differential regulation of the N-methyl-D-aspartate receptor by phencyclidine during development .” 2005. Thesis, University of Texas Medical Branch – Galveston. Accessed October 22, 2017. http://hdl.handle.net/2152.3/170.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7th Edition):

author], [No. “Regional and temporal differential regulation of the N-methyl-D-aspartate receptor by phencyclidine during development .” 2005. Web. 22 Oct 2017.

Vancouver:

author] [. Regional and temporal differential regulation of the N-methyl-D-aspartate receptor by phencyclidine during development . [Internet] [Thesis]. University of Texas Medical Branch – Galveston; 2005. [cited 2017 Oct 22]. Available from: http://hdl.handle.net/2152.3/170.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

author] [. Regional and temporal differential regulation of the N-methyl-D-aspartate receptor by phencyclidine during development . [Thesis]. University of Texas Medical Branch – Galveston; 2005. Available from: http://hdl.handle.net/2152.3/170

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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